chronic gastric bleeding
Introduction
Introduction Patients with chronic superficial gastritis have been in a state of congestion, edema, punctiform hemorrhage and erosion due to their gastric mucosa. Lightly aggravate the damage of the gastric mucosa, make the upper abdomen discomfort, nausea, vomiting worse; severely cause gastric ulcer and undetectable stomach bleeding, so that patients unconsciously have anemia, physical decline, low resistance, easy to concurrent other illnesses. The pathogenic factors of chronic superficial gastritis have not yet been fully understood. It has been found that almost any factor that can affect the body can cause chronic superficial gastritis.
Cause
Cause
The pathogenic factors of chronic superficial gastritis have not yet been fully understood. It has been found that almost any factor that can affect the body can cause chronic superficial gastritis. Among the more obvious causes are:
(1) Bacteria, viruses and toxins: more common after acute gastritis, gastric mucosal lesions have prolonged unhealed or repeated episodes, gradually evolved into chronic superficial gastritis.
(2) chronic infection of the nasal cavity, mouth and throat: chronic infections of the nasal cavity, mouth, pharynx, etc., such as long-term ingestion of bacteria or toxins such as alveolar pus, tonsillitis, sinusitis, etc., can repeatedly stimulate the gastric mucosa And cause chronic superficial gastritis. Chronic inflammatory changes were found in the stomach of 90% of patients with chronic tonsillitis.
(3) Smoking: The main harmful component in tobacco is nicotine. Long-term heavy smoking can relax the pyloric sphincter, duodenal fluid reflux, and gastric vasoconstriction, increase gastric acid secretion, thereby destroying the gastric mucosal barrier and causing chronic inflammatory lesions. . According to Eward, 40% of people who smoke more than 20 cigarettes a day can develop inflammation of the gastric mucosa.
(4) drugs: certain drugs such as salicylic acid preparations, corticosteroids, digitalis, indomethacin, phenylbutazone, etc., can cause chronic gastric mucosal damage.
(5) Irritant foods: Long-term consumption of spirits, tea, coffee, spicy and rough foods, as well as irregular eating patterns such as hunger or satiety can destroy the gastric mucosal protective barrier and produce gastritis.
(6) Circulatory and metabolic dysfunction: The structural and functional integrity of the gastric mucosa and its ability to defend against various damaging factors are closely related to adequate mucosal blood flow. In patients with congestive heart failure or portal hypertension, the stomach is in a state of blood stasis and hypoxia for a long time, resulting in a weakening of the gastric mucosal barrier function, a decrease in gastric acid secretion, and a large number of bacteria, which may easily cause inflammatory damage of the gastric mucosa. In chronic renal failure, urea is excreted from the gastrointestinal tract, and ammonium carbonate and ammonia are produced by bacteria or intestinal hydrolase, causing irritative damage to the gastric mucosa, resulting in congestion and edema of the gastric mucosa, and even erosion.
(7) Bile or duodenal reflux: The discovery or confirmation of bile reflux by fiberoptic endoscopy is an important cause of chronic gastritis. Due to dysfunction of the pyloric sphincter or duodenal juice or bile after gastric surgery, it can reflux into the stomach and destroy the gastric mucosal barrier, which promotes the reverse diffusion of H?+ and pepsin into the mucosa, causing a series of pathological reactions, leading to chronic gastritis. .
(8) Helicobacter pylori (HP) infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the gastric mucosal layer and epithelial cells of patients with chronic gastritis. Since then, many scholars have carried out a large number of experimental studies on patients with chronic gastritis, HP is cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis, and then it is found that the degree of HP infection is positively correlated with the degree of inflammation of the gastric mucosa. Therefore, in 1986, the eighth session of the World Gastroenterology Society proposed that HP infection is one of the important causes of chronic gastritis. The pathogenesis of HP may be mainly caused by destroying the gastric mucosal barrier and causing H+ to diffuse in the opposite direction, eventually causing inflammation of the gastric mucosa.
(9) Psychosomatic factors: Because mental health is unhealthy, long-term mental stress, anxiety or depression can cause imbalance of systemic sympathetic and parasympathetic functions. In particular, the sympathetic nerves are in an excitatory state for a long time, which may also lead to vasomotor dysfunction of the gastric mucosa, resulting in a decrease in blood flow of the gastric mucosa, destroying the barrier function of the gastric mucosa, and forming a chronic inflammatory reaction of the gastric mucosa over time.
Examine
an examination
Related inspection
Gastrointestinal CT examination gastroscope
Abdominal pain is the most common symptom in chronic superficial gastritis, and some patients may have no symptoms. The clinical manifestations are as follows:
1. Upper abdominal pain: The pain is irregular and has nothing to do with diet. It is usually diffuse upper abdomen burning pain, dull pain, pain and so on. Very few patients show colic and radiate to the back, which is easily misdiagnosed as angina pectoris.
2. Hernia: Due to lack of stomach acid, gas fermentation in the stomach and other factors make the gas in the stomach, resulting in hernia.
3. Abdominal distension: bloating occurs due to food retention, delayed emptying, indigestion, and eating foods that are not easily digested.
4. Loss of appetite: chronic superficial gastritis has a loss of appetite or good or bad.
5. Nausea and vomiting: inflammatory gastric mucosa acceptance, biological factors stimulation, as well as gastric dysfunction, stomach reverse peristalsis, nausea and vomiting.
6. Constipation and diarrhea: Most patients have constipation symptoms and relatively few diarrhea.
Diagnostic tests can be based on the above clinical manifestations.
Diagnosis
Differential diagnosis
Should be differentiated from acute gastritis:
Acute gastritis is a common disease, mainly manifested as upper abdominal pain, discomfort, loss of appetite, nausea and vomiting, sometimes accompanied by diarrhea. Severe acute gastritis can also cause hematemesis and blood in the stool.
The performance of superficial gastritis:
1 The mucus is attached to the mucous membrane and is not easy to fall off. After washing with water, the surface of the mucous membrane is red or erosive and exfoliated. It needs to be differentiated from the mucous membrane of the swallow or the duodenal reflux mucus. Generally, the reflux mucus contains air bubbles and creeps. And move.
2 small patchy or linear red, some places are congested, and some places are not congested, so it is plaque-like, the redness of the realm is not very obvious, the color is bright red. Linear congestion is common in wrinkled wall ridges.
3 red and white or spotted, is a small red dot scattered evenly, the mucosa between the red dot and the black spot is slightly pale, a bit like the skin of children with measles, the general mucosa is relatively flat.
4 edema, mucus reflective, slightly pale, swelling.
5 erosive surface mucosal exfoliation, often white moss, can be divided into three types: uplift type, such as papule-like apex at the top; flat type, not higher than the surrounding mucosa; concave invisible, lower than the surrounding mucosa. The erosive surrounding mucosa often has an inflammatory manifestation.
The performance of atrophic gastritis:
1 mucosa color change: normal orange-red, gray, gray-yellow, gray or gray-green when atrophy; the mucosa in the same part is inconsistent, the red strong place is also grayish white, generally grayish yellow or grayish white also has a small bulge Red spots or erythema exist; the range of atrophic mucosa can be diffuse, local, or even small, the mucosa becomes thin and sag, and the boundary is often not obvious.
2 vascular permeability: small blood vessels in the mucosa can be seen at the beginning of atrophy; heavy vessels under the mucosa such as dendrites, dark red, sometimes as if on the mucosal surface, easily mixed with wrinkles; normal blood vessels of the fundus It can also be seen that the pressure in the stomach should be mastered when observing blood vessels. Atrophic gastritis can also be combined with superficial gastritis; after glandular atrophy, the glandular fossa can proliferate or prolong the intestinal metaplasia and the formation of the mucosa becomes thicker. At this time, the submucosal blood vessels can not be seen, only the mucosa can be seen. The surface is rough, the particles or nodules are stiff, and the gloss is also changed.
Abdominal pain is the most common symptom in chronic superficial gastritis, and some patients may have no symptoms. The clinical manifestations are as follows:
1. Upper abdominal pain: The pain is irregular and has nothing to do with diet. It is usually diffuse upper abdomen burning pain, dull pain, pain and so on. Very few patients show colic and radiate to the back, which is easily misdiagnosed as angina pectoris.
2. Hernia: Due to lack of stomach acid, gas fermentation in the stomach and other factors make the gas in the stomach, resulting in hernia.
3. Abdominal distension: bloating occurs due to food retention, delayed emptying, indigestion, and eating foods that are not easily digested.
4. Loss of appetite: chronic superficial gastritis has a loss of appetite or good or bad.
5. Nausea and vomiting: inflammatory gastric mucosa acceptance, biological factors stimulation, as well as gastric dysfunction, stomach reverse peristalsis, nausea and vomiting.
6. Constipation and diarrhea: Most patients have constipation symptoms and relatively few diarrhea.
Diagnostic tests can be based on the above clinical manifestations.
